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XIO > Upper GI 2 > Flashcards

Upper GI 2 Flashcards

1
Q

hiatal hernia - more common in who?

A

Most common abnormality found on upper GI x-ray
■ More common in older adults and women

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2
Q

2 types of hiatal hernia (hernias slide in pairs)

A

sliding and Paraesophageal or rolling

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3
Q

sliding hernia (the slide goes down)

A

slides into stomach when pt is lying down

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4
Q

Paraesophageal or rolling hernia

A

Fundus and greater curvature of stomach roll up through diaphragm, forming a pocket alongside the esophagus

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5
Q

Acute paraesophageal hernia is a (a cute para needs a paramedic)

A

medical emergency

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6
Q

hiatal hernia - causes (big)

A

Structural changes occur with aging
▪ Weakening of muscles in diaphragm ▪ Increased intraabdominal pressure
▪ Obesity
▪ Pregnancy
▪ Heavy lifting

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7
Q

hiatal hernia - symptoms (Hernia - H)

A

May be asymptomatic
▪ Symptoms include
▪ Heartburn
▪ After meal or when lying supine
▪ Dysphagia

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8
Q

hiatal hernia - complications

A

■ GERD
■ Esophagitis
■ Hemorrhage from erosion
■ Stenosis
■ Ulcerations of herniated portion
■ Strangulation of the hernia
■ Regurgitation with tracheal aspiration
■ Increased risk of respiratory problems

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9
Q

hiatal hernia - diagnostics (the only 2 you know)

A

Esophagogram (barium swallow) and endoscopy

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10
Q

hiatal hernia - management - conservative therapy (and what meds?)

A

ConservativeTherapy
▪ Lifestyle modifications
▪ Eliminate alcohol
▪ Elevate head of bed
▪ Smoking cessation
▪ Avoid lifting/straining
▪ Reduce weight, if appropriate
▪ Use antisecretory agents and antacids

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11
Q

esophageal diverticula (divert the zinc w/ traction and epinephrine)

A

Occur in 3 main areas
1. Zenker’s diverticulum
▪ Most common location
▪ Above the upper esophageal sphincter 2. Traction diverticulum
▪ Near esophageal midpoint 3. Epiphrenic diverticulum
▪ Above the LES

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12
Q

Esophageal Diverticula Clinical Manifestations (same a gerd)

A

■ Dysphagia
■ Regurgitation
■ Chronic cough
■ Aspiration
■ Weight loss

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13
Q

Esophageal Diverticula Complications (the MAP diverts up)

A

■ Malnutrition
■ Aspiration
■ Perforation

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14
Q

Esophageal Diverticula Diagnostic Studies (the same 2)

A

■ Endoscopy
■ Barium studies

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15
Q

Esophageal Diverticula Interprofessional Care (touch neck)

A

■ Applying pressure at a point on neck to empty pocket of food
■ Diet may need to be limited to foods that are blenderized
■ Treatment may be necessary if nutrition disrupted
■ Surgery
▪ Endoscopic or open approach (associated w/ morbitidy - usually older ppl)
▪ Most serious complication is esophageal perforation

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16
Q

Esophageal Strictures - over long or short time?

A

Usually develop over a long time

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17
Q

Esophageal Strictures - causes - most common? (Gerdie is #1 strict)

A

▪ GERD: most common cause
▪ Ingestion of strong acids or alkalis ▪ External beam radiation
▪ Surgical anastamosis
▪ Trauma

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18
Q

Esophageal Strictures - manifestations (DRW has strictures)

A

▪ Dysphagia
▪ Regurgitation
▪ Weight loss

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19
Q

Esophageal Strictures - treatment

A

▪ Dilated endoscopically ▪ Surgical excision
▪ Patient may have a temporary or a permanent gastrostomy (opening in stomach)

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20
Q

Achalasia (atcha is paralyzed)

A

▪ Rare, chronic disorder
▪ Exact cause is unknown
▪ Peristalsis is absent in lower 2/3 of esophagus
LES pressure ↑

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21
Q

Achalasia - manifestations (atcha can’t swallow w/ a lump in her throat)

A

▪ Dysphagia
▪ Most common symptom
▪ Liquids and solids
▪ Globus sensation (lump in throat)
▪ Substernal chest pain
▪ During/after a meal

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22
Q

Achalasia Diagnostic Studies

A

▪ Esophagogram (barium swallow)
▪ Manometric studies of lower esophagus
▪ Endoscopy

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23
Q

Achalasia - treatment - Endoscopic pneumatic dilation (atcha needs balloons)

A

▪ Outpatient procedure
▪ Dilation of LES using balloons of progressively larger diameters
▪ Repeat dilations are often required

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24
Q

Achalasia - Symptomatic relief (drink water with meals, back atcha)

A

▪ Semisoft diet ▪ Eating slowly
▪ Drinking with meals
▪ Sleeping with head of bed elevated

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25
Q

Esophageal Varices (varices is varacose) what is the cause?

A

Dilated, tortuous veins at the lower end of the esophagus caused by portal HTN

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26
Q

Esophageal Varices - Large varices are more likely to

A

bleed.

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27
Q

Ruptured esophageal varices are the

A

the most life- threatening complication of cirrhosis and considered a medical emergency.

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28
Q

Peptic Ulcer Disease

A

Erosion of GI mucosa resulting from digestive action of HCl acid and pepsin

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29
Q

peptic ulcers can occur in (pepi is in the LSD)

A

▪ Lower esophagus
▪ Stomach
▪ Duodenum
▪ Margin of gastrojejunal anastomosis after surgical procedures

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30
Q

acute peptic ulcer - heal fast or slow?

A

▪ Superficial erosion
▪ Minimal inflammation
▪ Short duration: resolves quickly when cause is identified and removed

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31
Q

chronic peptic ulcer - how long? and are they common?

A

▪ Long duration
▪ Muscular wall erosion with formation of fibrous tissue
▪ Present continuously for many months or intermittently throughout person’s lifetime
▪ More common than acute erosions

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32
Q

peptic ulcers - patho

A

■ Develop only in presence of an acid environment
■ Excess HCl may not be necessary for ulcer development
■ Pepsinogen converts to pepsin in presence of HCl acid and at pH of 2 to 3
■ pH increases to 3.5 or more when
– Food or antacids neutralize the stomach acid
– Drugs block acid secretion
■ Back diffusion of HCl acid into gastric mucosa results in cellular destruction and inflammation
■ Histamine is released from damaged mucosa
■ Causes vasodilation, increased capillary permeability and further secretion of acid and pepsin

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33
Q

Destroyers of mucosal barrier: - Helicobacter pylori (helicopter is ur ease)

A

Helicobacter pylori (2/3 of world’s pop is infected)
▪ Major risk factor for PUD
▪ Produces enzyme urease
▪ Urease activates immune response
▪ Antibody production
▪ Release of inflammatory cytokines
▪ Leads to increased gastric secretions and causes damage

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34
Q

Destroyers of mucosal barrier: NSAIDs and aspirin

A

▪ Inhibit prostaglandin synthesis
▪ Increase gastric acid secretion
▪ Reduce integrity of the mucosal barrier
▪ Responsible for majority of non-H. pylori peptic ulcers
▪ NSAIDs in presence of H. pylori increase risk of PUD

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35
Q

Destroyers of mucosal barrier: steroids (steroids shrink)

A

▪ ↓ Rate of mucosal cell renewal
▪ ↓ Protective effects

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36
Q

Gastric Ulcers (gastric ulcers go everywhere in the stomach) and who gets them? (women stress)

A

■ Occur in any portion of stomach
■ Less common than duodenal ulcers
■ More prevalent in women
■ Peak incidence >50 years of age
■ More likely than duodenal ulcers to result in obstruction

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37
Q

gastric ulcers - risk factors (3 things) HMR (gassy hummer)

A

▪ H. pylori
▪ Medications
▪ Bile reflux

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38
Q

Duodenal Ulcers (duo is prevalent and young)

A

▪ Account for ~80% of all peptic ulcers
▪ Occur at any age and in anyone
▪ ↑ Between ages of 35 and 45 years
▪ H. pylori is found in 90% to 95% of patients
▪ Associated with increased HCl acid secretion

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39
Q

Duodenal Ulcers - Increased risk: (Dua and Zellwiger have ulcers at the door)

A

▪ COPD
▪ Cirrhosis of liver
▪ Chronic pancreatitis
▪ Hyperparathyroidism
▪ Chronic kidney disease
▪ Zollinger-Ellison syndrome

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40
Q

stress-Related Mucosal Disease (SRMD) (this surgery and trauma is stressing me)

A

■ Also called physiologic stress ulcer
■ Acute ulcers that develop after major physiologic insult
▪ Trauma or surgery

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41
Q

Gastric ulcers - manifestations- pain how long after meals?

A

▪ Pain generally high in epigastrium
▪ 1–2 hours after meals
▪ “Burning” or “gaseous”
▪ Food aggravates pain if ulcer has eroded through gastric mucosa

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42
Q

Duodenal ulcer - manifestations - pain how long after meals? (Dua is 25)

A

▪ Pain in midepigastric region beneath xiphoid process
▪ Back pain—if ulcer is located in posterior aspect
▪ 2–5 hours after meals
▪ “Burning” or “cramplike”
▪ Tendency to occur, then disappear, then occur again

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43
Q

Gastric ulcer - G

A

great pain

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44
Q

Duadenal ulcer - D

A

decrease pain

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45
Q

3 complications with ulcers (think if they rip off or block)

A

▪ Hemorrhage
▪ Perforation
▪ Gastric outlet obstruction
▪ All considered emergency situations

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46
Q

hemmorhage - does pain increase or decrease?

A

▪ Most common complication of PUD
▪ Dudoenal ulcers cause more UGIB (upper GI bleeds) episodes than gastric ulcers
▪ Clinical Manifestations:
▪ Changes in vital signs, ↑ in amount and redness of aspirate ▪ Signals massive upper GI bleeding
▪ ↑ Amount of blood in gastric contents
▪ ↓ Pain because blood neutralizes acidic gastric contents

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47
Q

Perforation

A

■ Occurs when ulcer penetrates serosal surface with spillage of contents into peritoneal cavity

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48
Q

manifestations of perforation - pain how quickly? and bowel sounds?

A

▪ Sudden, dramatic onset
▪ Initial phase (0–2 hours after perforation)
▪ Sudden, severe upper abdominal pain- quickly spreads throughout abdomen ▪ Pain radiates to back
▪ Rigid, boardlike abdominal muscles
▪ Shallow, rapid respirations
▪ Tachycardia, weak pulse
▪ Bowel sounds absent
▪ Nausea/vomiting

49
Q

perforation treatment

A

▪ Immediate focus:
▪ Stop spillage of gastric or duodenal contents into peritoneal cavity
▪ Restore blood volume ▪ NG tube
▪ IVF
▪ pRBCs may be necessary
▪ ECG if patient has history of cardiac disease ▪ Broad-spectrum antibiotics
▪ Open or laparoscopic repair

50
Q

Gastric Outlet Obstruction (Distal stomach and duodenum obstruction is the result…)

A

■ Acute and chronic PUD can result in gastric outlet obstruction
■ Distal stomach and duodenum obstruction is the result of: ▪ Edema
▪ Inflammation
▪ Pylorospasm and fibrous scar tissue formation

51
Q

Gastric Outlet Obstruction - Clinical manifestations: (projectile vomiting at the outlet mall) and when is pain worse?

A

▪ Pain worsens toward end of day as stomach fills and dilates ▪ Relief obtained by belching or vomiting
▪ Vomiting is common, often projectile

52
Q

Gastric Outlet Obstruction - treatment

A

▪ Decompress stomach via NGT
▪ Correct any existing fluid and electrolyte imbalances
▪ PPI or H2 receptor blocker if obstruction due to active ulcer ▪ Balloon dilation for pyloric obstruction
▪ Surgery may be needed to remove scar tissue

53
Q

PUD - diagnostic studies

A

Endoscopy with biopsy
▪ Most often used as it allows for
direct viewing of mucosa
▪ Tissue specimens can be obtained to identify H. pylori and rule out stomach cancer
▪ Determine degree of ulcer healing after treatment

54
Q

PUD - diagnostic studies - non-invasive (pugs have urea on their breath)

A

Noninvasive tests for H. pylori ▪ Urea breath test
▪ Can determine active infection
▪ Stool antigen test
▪ Serum or whole blood antibody tests
▪ Immunoglobin G (IgG)
▪ Will not distinguish between past and current infection

55
Q

PUD - diagnostic studies - invasive

A

Invasive tests for H. pylori infection ▪ Endoscopic procedure
▪ Biopsy of stomach
▪ Rapid urease testing

56
Q

PUD diagnostic - con’t

A

Barium contrast study
▪ Reserved for patient who cannot
undergo endoscopy
▪ Not accurate for shallow, superficial ulcers
▪ Used in diagnosis of gastric outlet obstruction
▪ Gastric analysis
▪ Analysis of gastric contents for
acidity and volume
▪ NG tube is inserted, and gastric contents are aspirated
▪ Contents analyzed for HCl acid

57
Q

PUD - labs (pud needs liver tests)

A

Laboratory analysis ▪ CBC
▪ Liver enzyme studies
▪ Serum amylase determination ▪ Stool examination for blood

58
Q

PUD treatment

A

▪ Adequate rest
▪ Drug therapy
▪ Smoking cessation
▪ Dietary modification
▪ Long-term follow-up care

59
Q

goal of PUD treatment

A

▪ Reduce degree of gastric acidity
▪ Enhance mucosal defense mechanisms

60
Q

PUD aftercare - how quickly does the pain subside?

A

▪ Generally treated in ambulatory care setting
▪ Pain disappears after 3–6 days
▪ Ulcer healing requires many weeks of therapy
▪ Endoscopic examination most accurate method to monitor healing

61
Q

PUD drug therapy

A

▪ PPIs
▪ H2R blockers
▪ Antibiotics
▪ Antacids
▪ Anticholinergics
▪ Cytoprotective therapy

62
Q

Antibiotic therapy to tx H. pylori: (pylori is tough)

A

▪ No single agent has been
effective in eliminating H. pylori
▪ Prescribed concurrently with a PPI for 14 days

63
Q

Antacids - what do they do? (the opposite of what you think)

A

▪ Adjunct therapy for PUD
▪ Increase gastric pH by neutralizing HCl acid

64
Q

Cytoprotective drug therapy - long or short term therapy?

A

Used for short-term treatment
▪ Protection for esophagus, stomach, and duodenum

65
Q

Cytoprotective drug therapy ex (socrates and miso protect my stomach)

A

▪ Sucralfate
▪ Misoprostol

66
Q

PUD - nutritional therapy (pugs eat anything)

A

■ No specific dietary modifications
■ Eat and drink foods and fluids that do not cause symptoms
■ Avoid alcohol use

67
Q

PUD nursing management - stool?

A

■ PMHx
■ Medication
■ Heartburn
■ Weight loss
■ Black, tarry stools
■ Epigastric tenderness
■ Nausea and vomiting
■ Abnormal laboratory values
■ Acute pain
■ Ineffective health management
■ Nausea

68
Q

PUD professional care

A

Vagotomy and Pyloroplasty

69
Q

PUD - most common post op complications (pugs get down in the dumps w/ low blood sugar and reflux)

A

▪ Dumping syndrome
▪ Postprandial hypoglycemia
▪ Bile reflux gastritis

70
Q

dumping syndrome - how many pts get it? and how long does it last?

A

Experienced by 20% of patients after PUD surgery. symptoms usually lasts less than 1 hour

71
Q

dumping syndrome

A

see other slide

72
Q

PUD - nutrition post op (pugs eat dry food, with low sugar after surgery)

A

▪ Small, dry feedings daily
▪ Low carbohydrates
▪ Restricted sugar with meals
▪ Moderate amounts of protein and fat

73
Q

PUD - Pernicious anemia is a long-term complication

A

▪ After total or partial gastrectomy
▪ Due to loss of intrinsic factor (substance that helps vitamin B12 be absorbed)
▪ Patient will require cobalamin replacement therapy

74
Q

PUD - geriatric considerations - what is the first symptom? (let’s be frank, it’s geriatric)

A

▪ ↑ Morbidity/mortality in older adults ▪ Concurrent health problems
▪ ↑ Use of NSAIDs
▪ First manifestation may be frank gastric bleeding or ↓ hematocrit ▪ Treatment similar to that for younger adults
▪ Emphasis placed on prevention

75
Q

Gastritis

A

■ Inflammation of gastric mucosa
■ One of most common problems affecting the stomach
■ May be acute or chronic
■ Result of a breakdown in gastric mucosal barrier
■ Stomach tissue unprotected from autodigestion by HCl acid and pepsin

76
Q

Gastritis - nsaids do what? (Prostie doesn’t like nsaids)

A

▪ Direct irritating effect on gastric mucosa
▪ NSAIDs, including aspirin and corticosteroids, inhibit
prostaglandin synthesis

77
Q

gastritis - Stomach acid and pepsin can (basically just get through)

A

diffuse back into the mucosa resulting in: ▪ Tissue edema
▪ Disruption of capillary walls
▪ With loss of plasma into gastric lumen ▪ Possible hemorrhage

78
Q

Risk factors for NSAID-induced gastritis (age and gender)

A

▪ Being female
▪ Being over age 60
▪ Hx of ulcer disease
▪ Anticoagulants, other NSAIDs, or ulcerogenic drugs
▪ Having a chronic debilitating disorder
▪ Diet
▪ ETOH
▪ Microorganisms
▪ H. pylori
▪ Important cause of chronic gastritis
▪ Promotes breakdown of gastric
mucosal barrier
▪ Bacterial, viral, and fungal infections

79
Q

Autoimmune atrophic gastritis - affects what area of the stomach? (atrophy in my body is fun)

A

▪ Affects fundus and body of stomach

80
Q

gastritis - risk factors con’t (vomiting?)

A

▪ Anatomic changes following surgical
procedures
▪ Prolonged vomiting
▪ Intense emotional responses
▪ CNS lesions

81
Q

acute gastritis - clinical manifestations (think of acute sickness) and common with group?

A

■ Anorexia
■ Nausea
■ Vomiting
■ Epigastric tenderness
■ Feeling of fullness
■ Hemorrhage
▪ Common with alcohol abuse ▪ May be only symptom

82
Q

Chronic Gastritis
Clinical Manifestations (same as acute)

A

▪ Symptoms are similar to those of acute gastritis
▪ Loss of intrinsic factor can occur when acid-secreting cells are lost or nonfunctioning
▪ Essential for absorption of cobalamin (vitamin B12)

83
Q

Acute gastritis - Diagnosis most often based on (think who gets acute)

A

patient’s symptoms and history of drug or alcohol use

84
Q

Chronic gastritis
▪ Diagnosis may be delayed or missed because of

A

nonspecific symptoms

85
Q

gastritis - Endoscopic examination with biopsy - is it necessary?

A

▪ Necessary for definitive diagnosis

86
Q

gastritis - Samples of what? (Gastritis gets every test)

A

Samples of breath, urine, serum, stool, and gastric tissue to determine H. pylori infection

87
Q

gastritis - Radiologic studies

A

Radiologic (x-rays) studies not helpful

88
Q

gastritis - CBC

A

▪ CBC
▪ Confirm presence of anemia from blood loss or lack of intrinsic factor
▪ Occult blood test
▪ Serum tests for antibody to parietal cells and intrinsic factor
▪ Tissue biopsy with cytologic examination ▪ Rule out gastric cancer

89
Q

chronic gastritis - care (not helpful)

A

Focuses on evaluating and eliminating specific cause

90
Q

UGIB - upper GI bleeding - Obvious bleeding
▪ Hematemesis (heman is fresh)

A

▪ Bloody vomitus
▪ Appears fresh, bright red blood or “coffee grounds”

91
Q

UGIB - upper GI bleeding - Melena (it’s in the name)

A

▪ Black, tarry stools
▪ Caused by digestion of blood in GI tract ▪ Black appearance—due to iron

92
Q

UGIB - upper GI bleeding - Occult bleeding

A

▪ Small amounts of blood in gastric secretions, vomitus, or stools ▪ Undetectable by appearance
▪ Detectable by guaiac test

93
Q

Esophageal origin - bleeding

A

– Chronic esophagitis
– GERD
– Mucosa-irritating drugs
– Smoking
– Alcohol use

94
Q

Stomach and duodenal origin - bleeding (think ulcers)

A

– Peptic ulcer disease
■ Bleeding ulcers account for 40% of cases of UGI bleeding
– Drugs
■ Aspirin, NSAIDs, corticosteroids

95
Q

– Stress-related mucosal disease (SRMD) - common among who?

A

■ Also called physiologic stress ulcers
■ Most common in critically ill patients
– Severe burns, trauma, or major surgery
– Patients with coagulopathy on mechanical ventilation

96
Q

upper GI bleed - diagnosis (you know if, and do you wash away the blood?)

A

Endoscopy
▪ Primary tool for diagnosing source of upper GI bleeding ▪ Before performing
▪ Lavage may be needed for clearer view
▪ NG or orogastric tube placed, and room-temperature water
or saline used
▪ Do not advance tube against resistance
▪ Stomach contents aspirated through a large-bore (Ewald) tube to remove clots

97
Q

upper GI bleed - diagostics - angiography - used when? (angie is the last resort)

A

Angiography
▪ Used to diagnose only when endoscopy cannot be done ▪ Invasive procedure
▪ May not be appropriate for high-risk or unstable patient
▪ Catheter placed into left gastric or superior mesenteric artery until site of bleeding is discovered

98
Q

Emergency Assessment and Management of UGIB - ▪ Immediate physical examination with focus on (think losing too much blood)!

A

BP
▪ Rate and character of pulse
▪ Peripheral perfusion with capillary refill ▪ Neurologic status

99
Q

Emergency Assessment and Management of UGIB - how often to assess output? (emergency every hour)

A

Indwelling urinary catheter for assessment of hourly output

100
Q

Emergency Assessment and Management of UGIB - tele

A

▪ Tele/CPO
▪ Central venous pressure line for assessment of fluid volume status ▪ Supplemental oxygen

101
Q

Emergency Assessment and Management of UGIB - abdonminal exam

A

▪ Presence or absence of bowel sounds
▪ Tense, rigid, boardlike abdomen: may indicate perforation and peritonitis

102
Q

Emergency Assessment and Management of UGIB - Type and amount of fluids infused are based on physical and laboratory findings (gi bleed is bore ing)

A

▪ 2 large bore IVs
▪ Isotonic crystalloid- Lactated Ringers ▪ Volume replacement
▪ Whole blood, packed red blood cells, fresh frozen plasma

103
Q

GI bleed - Endoscopic hemostasis therapy

A

▪ First-line therapy of upper GI bleed
▪ Goal: to coagulate or thrombose the bleeding vessel
▪ Useful for gastritis, Mallory-Weiss tear, esophageal and gastric varices, bleeding peptic ulcers, and polyps

104
Q

GI bleed - surgical therapy

A

▪ Indicated when bleeding continues
▪ Regardless of therapy provided
▪ Site of bleeding identified

105
Q

GI bleed - surgery may be needed if how much blood loss?

A

May be necessary when
▪ Patient continues to bleed after rapid transfusion of up to 2000 mL whole blood
▪ Remains in shock after 24 hours

106
Q

GI bleed - acute phase -what are drugs used for? (Just 2 things)

A

During acute phase, used to
▪ ↓Bleeding
▪ ↓ HCl acid secretion
▪ Neutralize HCl acid that is present

107
Q

upper GI bleeding - injection therapy

A

with epinephrine during endoscopy for acute hemostasis
▪ For bleeding due to ulceration
▪ Produces tissue edema → pressure on bleeding source

108
Q

upper GI bleed - Somatostatin (inhibits gi secretions)

A

▪ Used for upper GI bleeding
▪ Reduces blood flow to GI organs and acid secretion
▪ Given in IV boluses for 3–7 days after onset of bleeding

109
Q

upper GI bleed - nursing management - Signs/symptoms of shock

A

▪ Low BP
▪ Rapid, weak pulse
▪ Increased thirst
▪ Cold, clammy skin
▪ Restlessness

110
Q

ulcer perforation - lethal or not? and common where?

A

■ Most lethal complication
■ Common in large penetrating duodenal ulcers
■ Perforated gastric ulcers often located on lesser curvature of stomach
■ Mortality rate associated with perforation of gastric ulcers is higher

111
Q

large perforations - surgery?

A

■ Large perforations need immediate surgical closure
■ Small perforations may spontaneously seal
themselves

112
Q

perforation - how quickly will bacterial peritonitis occur?

A

▪ Bacterial peritonitis may occur within 6–12 hours
▪ Difficult to determine from symptoms alone if gastric or duodenal ulcer has perforated ▪ Manifestations of peritonitis are the same

113
Q

PUD aftercare - how long after can you take Aspirin and nonselective NSAIDs?

A

▪ Aspirin and nonselective NSAIDs are discontinued for 4–6 weeks
▪ Patients receiving low dose aspirin may need long-term PPI treatment

114
Q

antacids - how long to start working? With and without food

A

▪ Effects on empty stomach in 20–30 minutes
▪ If drugs taken after meals, effects may last 3–4 hours

115
Q

antacids and sodium

A

▪ ↑ Sodium preparations: used cautiously in older patients and patients with ↑BP, heart failure, liver cirrhosis, or renal disease
▪ Magnesium preparations: not to be used in patients with renal failure
▪ Can enhance or decrease the absorption of some drugs

116
Q

autoimmune atrophic gastritis - Associated with (and linked with what?) I can atrophy my cancer and h pylori

A

increased risk of gastric cancer
▪ May be linked to presence of H. pylori and development of autoimmune chronic gastritis`

117
Q

atchalsia - symptoms (atcha has bad breath and can’t burp)

A

▪ Halitosis
▪ Inability to belch
▪ GERD
▪ Regurgitation
▪ Weight loss

118
Q

gastric outlet obstruction - symptoms (can’t poop at the outlet mall)

A

▪ Constipation is a common complaint
▪ Dehydration
▪ Decreased dietary intake
▪ Anorexia
▪ Swelling in stomach and upper abdomen

XIO (372 decks)

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